ALBERT

Description: The supernova (SN) PTF11iqb was initially classified as a Type IIn event caught very early after explosion. It showed narrow Wolf–Rayet (WR) spectral features on day 2 (as in SN 1998S and SN 2013cu), but the narrow emission weakened quickly and the spectrum morphed to resemble Types II-L and II-P. At late times, Hα exhibited a complex, multipeaked profile reminiscent of SN 1998S. In terms of spectroscopic evolution, we find that PTF11iqb was a near twin of SN 1998S, although with somewhat weaker interaction with circumstellar material (CSM) at early times, and stronger interaction at late times. We interpret the spectral changes as caused by early interaction with asymmetric CSM that is quickly (by day 20) enveloped by the expanding SN ejecta photosphere, but then revealed again after the end of the plateau when the photosphere recedes. The light curve can be matched with a simple model for CSM interaction (with a mass-loss rate of roughly 10 –4  M  yr –1 ) added to the light curve of a normal SN II-P. The underlying plateau requires a progenitor with an extended hydrogen envelope like a red supergiant at the moment of explosion, consistent with the slow wind speed (〈80 km s –1 ) inferred from narrow Hα emission. The cool supergiant progenitor is significant because PTF11iqb showed WR features in its early spectrum – meaning that the presence of such WR features does not necessarily indicate a WR-like progenitor. Overall, PTF11iqb bridges SNe IIn with weaker pre-SN mass-loss seen in SNe II-L and II-P, implying a continuum between these types.

Description: We present photometric and spectroscopic observations of SN 2013fc, a bright type II supernova (SN) in a circumnuclear star-forming ring in the luminous infrared galaxy ESO 154-G010, observed as part of the Public ESO Spectroscopic Survey of Transient Objects. SN 2013fc is both photometrically and spectroscopically similar to the well-studied type IIn SN 1998S and to the bright type II-L SN 1979C. It exhibits an initial linear decline, followed by a short plateau phase and a tail phase with a decline too fast for 56 Co decay with full -ray trapping. Initially, the spectrum was blue and featureless. Later on, a strong broad (~8000 km s –1 ) H α emission profile became prominent. We apply a starlight stellar population model fit to the SN location (observed when the SN had faded) to estimate a high extinction of A V = 2.9 ± 0.2 mag and an age of $10_{-2}^{+3}$  Myr for the underlying cluster. We compare the SN to SNe 1998S and 1979C and discuss its possible progenitor star considering the similarities to these events. With a peak brightness of B = –20.46 ± 0.21 mag, SN 2013fc is 0.9 mag brighter than SN 1998S and of comparable brightness to SN 1979C. We suggest that SN 2013fc was consistent with a massive red supergiant (RSG) progenitor. Recent mass loss probably due to a strong RSG wind created the circumstellar matter illuminated through its interaction with the SN ejecta. We also observe a near-infrared excess, possibly due to newly condensed dust.

Description: IRE1 couples endoplasmic reticulum unfolded protein load to RNA cleavage events that culminate in the sequence-specific splicing of the Xbp1 mRNA and in the regulated degradation of diverse membrane-bound mRNAs. We report on the identification of a small molecule inhibitor that attains its selectivity by forming an unusually stable Schiff base with lysine 907 in the IRE1 endonuclease domain, explained by solvent inaccessibility of the imine bond in the enzyme-inhibitor complex. The inhibitor (abbreviated 4μ8C) blocks substrate access to the active site of IRE1 and selectively inactivates both Xbp1 splicing and IRE1-mediated mRNA degradation. Surprisingly, inhibition of IRE1 endonuclease activity does not sensitize cells to the consequences of acute endoplasmic reticulum stress, but rather interferes with the expansion of secretory capacity. Thus, the chemical reactivity and sterics of a unique residue in the endonuclease active site of IRE1 can be exploited by selective inhibitors to interfere with protein secretion in pathological settings.

Description: We present an investigation of the optical spectra of 264 low-redshift ( z 〈 0.2) Type Ia supernovae (SNe Ia) discovered by the Palomar Transient Factory, an untargeted transient survey. We focus on velocity and pseudo-equivalent width measurements of the Si ii 4130, 5972, and 6355 Å lines, as well those of the Ca ii near-infrared (NIR) triplet, up to +5 days relative to the SN B -band maximum light. We find that a high-velocity component of the Ca ii NIR triplet is needed to explain the spectrum in ~95 per cent of SNe Ia observed before –5 days, decreasing to ~80 per cent at maximum. The average velocity of the Ca ii high-velocity component is ~8500 km s –1 higher than the photospheric component. We confirm previous results that SNe Ia around maximum light with a larger contribution from the high-velocity component relative to the photospheric component in their Ca ii NIR feature have, on average, broader light curves and lower Ca ii NIR photospheric velocities. We find that these relations are driven by both a stronger high-velocity component and a weaker contribution from the photospheric Ca ii NIR component in broader light curve SNe Ia. We identify the presence of C ii in very-early-time SN Ia spectra (before –10 days), finding that 〉40 per cent of SNe Ia observed at these phases show signs of unburnt material in their spectra, and that C ii features are more likely to be found in SNe Ia having narrower light curves.

Description: We present a census of the active black hole population at 1 〈  z  〈 2, by constructing the bivariate distribution function of black hole mass and Eddington ratio, employing a maximum likelihood fitting technique. The study of the active black hole mass function (BHMF) and the Eddington ratio distribution function (ERDF) allows us to clearly disentangle the active galactic nuclei (AGN) downsizing phenomenon, present in the AGN luminosity function, into its physical processes of black hole mass downsizing and accretion rate evolution. We are utilizing type-1 AGN samples from three optical surveys (VVDS, zCOSMOS and SDSS), that cover a wide range of 3 dex in luminosity over our redshift interval of interest. We investigate the cosmic evolution of the AGN population as a function of AGN luminosity, black hole mass and accretion rate. Compared to z  = 0, we find a distinct change in the shape of the BHMF and the ERDF, consistent with downsizing in black hole mass. The active fraction or duty cycle of type-1 AGN at z  ~ 1.5 is almost flat as a function of black hole mass, while it shows a strong decrease with increasing mass at z  = 0. We are witnessing a phase of intense black hole growth, which is largely driven by the onset of AGN activity in massive SMBHs (supermassive black holes) towards z  = 2. We finally compare our results to numerical simulations and semi-empirical models and while we find reasonable agreement over certain parameter ranges, we highlight the need to refine these models in order to match our observations.

Description: Reports of substantial evidence for genetic linkage of schizophrenia to chromosome 1q were evaluated by genotyping 16 DNA markers across 107 centimorgans of this chromosome in a multicenter sample of 779 informative schizophrenia pedigrees. No significant evidence was observed for such linkage, nor for heterogeneity in allele sharing among the eight individual samples. Separate analyses of European-origin families, recessive models of inheritance, and families with larger numbers of affected cases also failed to produce significant evidence for linkage. If schizophrenia susceptibility genes are present on chromosome 1q, their population-wide genetic effects are likely to be small.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levinson, Douglas F -- Holmans, Peter A -- Laurent, Claudine -- Riley, Brien -- Pulver, Ann E -- Gejman, Pablo V -- Schwab, Sibylle G -- Williams, Nigel M -- Owen, Michael J -- Wildenauer, Dieter B -- Sanders, Alan R -- Nestadt, Gerald -- Mowry, Bryan J -- Wormley, Brandon -- Bauche, Stephanie -- Soubigou, Stephane -- Ribble, Robert -- Nertney, Deborah A -- Liang, Kung Yee -- Martinolich, Laura -- Maier, Wolfgang -- Norton, Nadine -- Williams, Hywel -- Albus, Margot -- Carpenter, Eric B -- DeMarchi, Nicola -- Ewen-White, Kelly R -- Walsh, Dermot -- Jay, Maurice -- Deleuze, Jean-Francois -- O'Neill, F Anthony -- Papadimitriou, George -- Weilbaecher, Ann -- Lerer, Bernard -- O'Donovan, Michael C -- Dikeos, Dimitris -- Silverman, Jeremy M -- Kendler, Kenneth S -- Mallet, Jacques -- Crowe, Raymond R -- Walters, Marilyn -- G9309834/Medical Research Council/United Kingdom -- G9810900/Medical Research Council/United Kingdom -- K24-MH64197/MH/NIMH NIH HHS/ -- KO2-01207/PHS HHS/ -- MH 41953/MH/NIMH NIH HHS/ -- MH 45390/MH/NIMH NIH HHS/ -- MH 52537/MH/NIMH NIH HHS/ -- MH61602/MH/NIMH NIH HHS/ -- R01-MH57314/MH/NIMH NIH HHS/ -- U01 MH46289/MH/NIMH NIH HHS/ -- U01 MH46318/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):739-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA. dfl@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976456" target="_blank"〉PubMed〈/a〉

Description: Stars with initial masses such that 10M[symbol: see text] 〈or= M(initial) 〈or= 100M[symbol: see text], where M[symbol: see text] is the solar mass, fuse progressively heavier elements in their centres, until the core is inert iron. The core then gravitationally collapses to a neutron star or a black hole, leading to an explosion-an iron-core-collapse supernova. By contrast, extremely massive stars with M(initial) 〉or= 140M[symbol: see text] (if such exist) develop oxygen cores with masses, M(core), that exceed 50M[symbol: see text], where high temperatures are reached at relatively low densities. Conversion of energetic, pressure-supporting photons into electron-positron pairs occurs before oxygen ignition and leads to a violent contraction which triggers a nuclear explosion that unbinds the star in a pair-instability supernova. Transitional objects with 100M[symbol: see text] 〈 M(initial) 〈 140M[symbol: see text] may end up as iron-core-collapse supernovae following violent mass ejections, perhaps as a result of brief episodes of pair instability, and may already have been identified. Here we report observations of supernova SN 2007bi, a luminous, slowly evolving object located within a dwarf galaxy. We estimate the exploding core mass to be M(core) approximately 100M[symbol: see text], in which case theory unambiguously predicts a pair-instability supernova. We show that 〉3M[symbol: see text] of radioactive (56)Ni was synthesized during the explosion and that our observations are well fitted by models of pair-instability supernovae. This indicates that nearby dwarf galaxies probably host extremely massive stars, above the apparent Galactic stellar mass limit, which perhaps result from processes similar to those that created the first stars in the Universe.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gal-Yam, A -- Mazzali, P -- Ofek, E O -- Nugent, P E -- Kulkarni, S R -- Kasliwal, M M -- Quimby, R M -- Filippenko, A V -- Cenko, S B -- Chornock, R -- Waldman, R -- Kasen, D -- Sullivan, M -- Beshore, E C -- Drake, A J -- Thomas, R C -- Bloom, J S -- Poznanski, D -- Miller, A A -- Foley, R J -- Silverman, J M -- Arcavi, I -- Ellis, R S -- Deng, J -- England -- Nature. 2009 Dec 3;462(7273):624-7. doi: 10.1038/nature08579.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Benoziyo Center for Astrophysics, Faculty of Physics, The Weizmann Institute of Science, Rehovot 76100, Israel. avishay.gal-yam@weizmann.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19956255" target="_blank"〉PubMed〈/a〉

Description: Schizophrenia, a devastating psychiatric disorder, has a prevalence of 0.5-1%, with high heritability (80-85%) and complex transmission. Recent studies implicate rare, large, high-penetrance copy number variants in some cases, but the genes or biological mechanisms that underlie susceptibility are not known. Here we show that schizophrenia is significantly associated with single nucleotide polymorphisms (SNPs) in the extended major histocompatibility complex region on chromosome 6. We carried out a genome-wide association study of common SNPs in the Molecular Genetics of Schizophrenia (MGS) case-control sample, and then a meta-analysis of data from the MGS, International Schizophrenia Consortium and SGENE data sets. No MGS finding achieved genome-wide statistical significance. In the meta-analysis of European-ancestry subjects (8,008 cases, 19,077 controls), significant association with schizophrenia was observed in a region of linkage disequilibrium on chromosome 6p22.1 (P = 9.54 x 10(-9)). This region includes a histone gene cluster and several immunity-related genes--possibly implicating aetiological mechanisms involving chromatin modification, transcriptional regulation, autoimmunity and/or infection. These results demonstrate that common schizophrenia susceptibility alleles can be detected. The characterization of these signals will suggest important directions for research on susceptibility mechanisms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775422/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775422/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Jianxin -- Levinson, Douglas F -- Duan, Jubao -- Sanders, Alan R -- Zheng, Yonglan -- Pe'er, Itsik -- Dudbridge, Frank -- Holmans, Peter A -- Whittemore, Alice S -- Mowry, Bryan J -- Olincy, Ann -- Amin, Farooq -- Cloninger, C Robert -- Silverman, Jeremy M -- Buccola, Nancy G -- Byerley, William F -- Black, Donald W -- Crowe, Raymond R -- Oksenberg, Jorge R -- Mirel, Daniel B -- Kendler, Kenneth S -- Freedman, Robert -- Gejman, Pablo V -- MC_U105292688/Medical Research Council/United Kingdom -- R01 AG037132/AG/NIA NIH HHS/ -- R01 MH059565/MH/NIMH NIH HHS/ -- R01 MH059565-08/MH/NIMH NIH HHS/ -- R01 MH059566/MH/NIMH NIH HHS/ -- R01 MH059566-08/MH/NIMH NIH HHS/ -- R01 MH059571/MH/NIMH NIH HHS/ -- R01 MH059571-08/MH/NIMH NIH HHS/ -- R01 MH059571-08S1/MH/NIMH NIH HHS/ -- R01 MH059586/MH/NIMH NIH HHS/ -- R01 MH059586-08/MH/NIMH NIH HHS/ -- R01 MH059587-09/MH/NIMH NIH HHS/ -- R01 MH059588-08/MH/NIMH NIH HHS/ -- R01 MH060870-09/MH/NIMH NIH HHS/ -- R01 MH060879/MH/NIMH NIH HHS/ -- R01 MH060879-08/MH/NIMH NIH HHS/ -- R01 MH061675/MH/NIMH NIH HHS/ -- R01 MH061675-09/MH/NIMH NIH HHS/ -- R01 MH061675-09S1/MH/NIMH NIH HHS/ -- R01 MH067257-04S1/MH/NIMH NIH HHS/ -- R01 MH081800/MH/NIMH NIH HHS/ -- R01 MH081800-01/MH/NIMH NIH HHS/ -- U01 MH046276/MH/NIMH NIH HHS/ -- U01 MH046276-08/MH/NIMH NIH HHS/ -- U01 MH046289-08/MH/NIMH NIH HHS/ -- U01 MH046318/MH/NIMH NIH HHS/ -- U01 MH046318-08/MH/NIMH NIH HHS/ -- U01 MH079469/MH/NIMH NIH HHS/ -- U01 MH079469-03/MH/NIMH NIH HHS/ -- U01 MH079470/MH/NIMH NIH HHS/ -- U01 MH079470-02/MH/NIMH NIH HHS/ -- U54 RR020278/RR/NCRR NIH HHS/ -- U54 RR020278-05/RR/NCRR NIH HHS/ -- England -- Nature. 2009 Aug 6;460(7256):753-7. doi: 10.1038/nature08192. Epub 2009 Jul 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, California 94304, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19571809" target="_blank"〉PubMed〈/a〉

Description: Autism spectrum disorders (ASDs) are childhood neurodevelopmental disorders with complex genetic origins. Previous studies focusing on candidate genes or genomic regions have identified several copy number variations (CNVs) that are associated with an increased risk of ASDs. Here we present the results from a whole-genome CNV study on a cohort of 859 ASD cases and 1,409 healthy children of European ancestry who were genotyped with approximately 550,000 single nucleotide polymorphism markers, in an attempt to comprehensively identify CNVs conferring susceptibility to ASDs. Positive findings were evaluated in an independent cohort of 1,336 ASD cases and 1,110 controls of European ancestry. Besides previously reported ASD candidate genes, such as NRXN1 (ref. 10) and CNTN4 (refs 11, 12), several new susceptibility genes encoding neuronal cell-adhesion molecules, including NLGN1 and ASTN2, were enriched with CNVs in ASD cases compared to controls (P = 9.5 x 10(-3)). Furthermore, CNVs within or surrounding genes involved in the ubiquitin pathways, including UBE3A, PARK2, RFWD2 and FBXO40, were affected by CNVs not observed in controls (P = 3.3 x 10(-3)). We also identified duplications 55 kilobases upstream of complementary DNA AK123120 (P = 3.6 x 10(-6)). Although these variants may be individually rare, they target genes involved in neuronal cell-adhesion or ubiquitin degradation, indicating that these two important gene networks expressed within the central nervous system may contribute to the genetic susceptibility of ASD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925224/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2925224/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glessner, Joseph T -- Wang, Kai -- Cai, Guiqing -- Korvatska, Olena -- Kim, Cecilia E -- Wood, Shawn -- Zhang, Haitao -- Estes, Annette -- Brune, Camille W -- Bradfield, Jonathan P -- Imielinski, Marcin -- Frackelton, Edward C -- Reichert, Jennifer -- Crawford, Emily L -- Munson, Jeffrey -- Sleiman, Patrick M A -- Chiavacci, Rosetta -- Annaiah, Kiran -- Thomas, Kelly -- Hou, Cuiping -- Glaberson, Wendy -- Flory, James -- Otieno, Frederick -- Garris, Maria -- Soorya, Latha -- Klei, Lambertus -- Piven, Joseph -- Meyer, Kacie J -- Anagnostou, Evdokia -- Sakurai, Takeshi -- Game, Rachel M -- Rudd, Danielle S -- Zurawiecki, Danielle -- McDougle, Christopher J -- Davis, Lea K -- Miller, Judith -- Posey, David J -- Michaels, Shana -- Kolevzon, Alexander -- Silverman, Jeremy M -- Bernier, Raphael -- Levy, Susan E -- Schultz, Robert T -- Dawson, Geraldine -- Owley, Thomas -- McMahon, William M -- Wassink, Thomas H -- Sweeney, John A -- Nurnberger, John I -- Coon, Hilary -- Sutcliffe, James S -- Minshew, Nancy J -- Grant, Struan F A -- Bucan, Maja -- Cook, Edwin H -- Buxbaum, Joseph D -- Devlin, Bernie -- Schellenberg, Gerard D -- Hakonarson, Hakon -- 1U24MH081810/MH/NIMH NIH HHS/ -- HD055751/HD/NICHD NIH HHS/ -- HD055782-01/HD/NICHD NIH HHS/ -- HD35476/HD/NICHD NIH HHS/ -- M01 RR000064-340579/RR/NCRR NIH HHS/ -- M01 RR000064-350579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10579/RR/NCRR NIH HHS/ -- M01 RR000064-35S10591/RR/NCRR NIH HHS/ -- M01 RR000064-35S10602/RR/NCRR NIH HHS/ -- M01 RR000064-35S20579/RR/NCRR NIH HHS/ -- M01 RR000064-35S20591/RR/NCRR NIH HHS/ -- M01 RR000064-35S20602/RR/NCRR NIH HHS/ -- M01 RR000064-360579/RR/NCRR NIH HHS/ -- M01 RR000064-360582/RR/NCRR NIH HHS/ -- M01 RR000064-360591/RR/NCRR NIH HHS/ -- M01 RR000064-36S10579/RR/NCRR NIH HHS/ -- M01 RR000064-36S10582/RR/NCRR NIH HHS/ -- M01 RR000064-36S10591/RR/NCRR NIH HHS/ -- M01 RR000064-370579/RR/NCRR NIH HHS/ -- M01 RR000064-370582/RR/NCRR NIH HHS/ -- M01 RR000064-370591/RR/NCRR NIH HHS/ -- M01 RR000064-37S10579/RR/NCRR NIH HHS/ -- M01 RR000064-37S10582/RR/NCRR NIH HHS/ -- M01 RR000064-37S10591/RR/NCRR NIH HHS/ -- M01 RR000064-380579/RR/NCRR NIH HHS/ -- M01 RR000064-380582/RR/NCRR NIH HHS/ -- M01 RR000064-380591/RR/NCRR NIH HHS/ -- M01 RR000064-390579/RR/NCRR NIH HHS/ -- M01 RR000064-390582/RR/NCRR NIH HHS/ -- M01 RR000064-390591/RR/NCRR NIH HHS/ -- M01-RR00064/RR/NCRR NIH HHS/ -- MH061009/MH/NIMH NIH HHS/ -- MH0666730/MH/NIMH NIH HHS/ -- MH64547/MH/NIMH NIH HHS/ -- MH69359/MH/NIMH NIH HHS/ -- NS049261/NS/NINDS NIH HHS/ -- P01 HD035476-03/HD/NICHD NIH HHS/ -- P01 HD035476-04/HD/NICHD NIH HHS/ -- P01 HD035476-04S1/HD/NICHD NIH HHS/ -- P01 HD035476-04S2/HD/NICHD NIH HHS/ -- P01 HD035476-05/HD/NICHD NIH HHS/ -- P50 HD055751/HD/NICHD NIH HHS/ -- P50 HD055751-01/HD/NICHD NIH HHS/ -- P50 HD055751-010002/HD/NICHD NIH HHS/ -- P50 HD055751-019003/HD/NICHD NIH HHS/ -- P50 HD055751-02/HD/NICHD NIH HHS/ -- P50 HD055751-020002/HD/NICHD NIH HHS/ -- P50 HD055751-03/HD/NICHD NIH HHS/ -- P50 HD055751-030002/HD/NICHD NIH HHS/ -- P50 HD055751-04/HD/NICHD NIH HHS/ -- P50 HD055782-01/HD/NICHD NIH HHS/ -- R01 MH057881/MH/NIMH NIH HHS/ -- R01 MH061009/MH/NIMH NIH HHS/ -- R01 MH061009-01A1/MH/NIMH NIH HHS/ -- R01 MH061009-01A1S1/MH/NIMH NIH HHS/ -- R01 MH061009-02/MH/NIMH NIH HHS/ -- R01 MH061009-03/MH/NIMH NIH HHS/ -- R01 MH061009-04A1/MH/NIMH NIH HHS/ -- R01 MH061009-05/MH/NIMH NIH HHS/ -- R01 MH061009-06/MH/NIMH NIH HHS/ -- R01 MH061009-07/MH/NIMH NIH HHS/ -- R01 MH061009-08/MH/NIMH NIH HHS/ -- R01 MH064547/MH/NIMH NIH HHS/ -- R01 MH064547-01/MH/NIMH NIH HHS/ -- R01 MH064547-01S1/MH/NIMH NIH HHS/ -- R01 MH064547-02/MH/NIMH NIH HHS/ -- R01 MH064547-02S1/MH/NIMH NIH HHS/ -- R01 MH064547-03/MH/NIMH NIH HHS/ -- R01 MH064547-04/MH/NIMH NIH HHS/ -- R01 MH064547-05/MH/NIMH NIH HHS/ -- R01 MH069359/MH/NIMH NIH HHS/ -- R01 MH069359-01A2/MH/NIMH NIH HHS/ -- R01 MH069359-02/MH/NIMH NIH HHS/ -- R01 MH069359-03/MH/NIMH NIH HHS/ -- R01 MH069359-04/MH/NIMH NIH HHS/ -- R01 MH069359-05/MH/NIMH NIH HHS/ -- R01 NS049261/NS/NINDS NIH HHS/ -- R01 NS049261-01A2/NS/NINDS NIH HHS/ -- R01 NS049261-02/NS/NINDS NIH HHS/ -- R01 NS049261-03/NS/NINDS NIH HHS/ -- R01 NS049261-04/NS/NINDS NIH HHS/ -- R01 NS049261-05/NS/NINDS NIH HHS/ -- U10 MH066766-02S1/MH/NIMH NIH HHS/ -- U10MH66766-02S1/MH/NIMH NIH HHS/ -- U19 HD035476-06/HD/NICHD NIH HHS/ -- U19 HD035476-07/HD/NICHD NIH HHS/ -- U19 HD035476-08/HD/NICHD NIH HHS/ -- U19 HD035476-09/HD/NICHD NIH HHS/ -- U19 HD035476-10/HD/NICHD NIH HHS/ -- U24 MH081810/MH/NIMH NIH HHS/ -- U24 MH081810-01/MH/NIMH NIH HHS/ -- U24 MH081810-02/MH/NIMH NIH HHS/ -- U24 MH081810-03/MH/NIMH NIH HHS/ -- U24 MH081810-04/MH/NIMH NIH HHS/ -- U54 MH066673/MH/NIMH NIH HHS/ -- U54 MH066673-01A10001/MH/NIMH NIH HHS/ -- U54 MH066673-020001/MH/NIMH NIH HHS/ -- U54 MH066673-030001/MH/NIMH NIH HHS/ -- U54 MH066673-040001/MH/NIMH NIH HHS/ -- U54 MH066673-05/MH/NIMH NIH HHS/ -- U54 MH066673-050001/MH/NIMH NIH HHS/ -- UL1 RR024134/RR/NCRR NIH HHS/ -- UL1 RR024134-03/RR/NCRR NIH HHS/ -- UL1-RR024134-03/RR/NCRR NIH HHS/ -- Medical Research Council/United Kingdom -- England -- Nature. 2009 May 28;459(7246):569-73. doi: 10.1038/nature07953. Epub 2009 Apr 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Applied Genomics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19404257" target="_blank"〉PubMed〈/a〉